Preload, also known as the left ventricular
end-diastolic pressure (LVEDP).It can be defined as the initial
stretching of the cardiac myocytes prior to contraction. Preload,
therefore, is related to muscule sarcomere length. Because
sarcomere length cannot be determined in the intact heart, other
indices of preload are used such as ventricular end-diastolic
volume or pressure.
When venous return to the heart is increased, the end-diastolic
pressure and volume of the ventricles are increased, which
stretches the sarcomeres, thereby increasing their preload.
Preload is increased by:
- Increased central venous pressurethat can result from decreased
venous compliance (e.g., caused by sympathetic activation of venous
smooth muscle) or increased thoracic blood volume. The latter can
be increased by either increased total blood volume or by venous
return augmented by increased respiratory activity,
increasedskeletal muscle pump activity, or by effects gravity
(e.g., head-down tilt).
- Increased ventricular compliance, which results in a greater
expansion of the chamber during filling at a given filling
- Increased atrial force of contraction resulting from
sympathetic stimulation of the atria or from increased filling of
the atria and therefore increased atrial contractile force through
the Frank-Starling mechanism.
- Reduced heart rate, which increasesventricular filling
- Increased aortic pressure, which increases the afterload on the
ventricle, reduces stroke volume by increasing end-systolic volume,
and leads to a secondary increase in ventricular preload.
- Pathological conditions such asventricular systolic failure and
valve defects such as aortic stenosis, andaortic regurgitation
(pulmonary valve stenosis and regurgitation have similar effects on
right ventricular preload).
- An arteriovenous fistula can increase preload.